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Steven Pinker gets his genome tested ...

"... and discovers he has the Bald Gene.

In a long article in the New York Times Magazine, "My Genome, My
Self," the author of The Blank Slate recounts all that he has learned
about himself from having his genome sampled, which turns out to be
unsurprisingly modest.

The most prominent finding of behavioral genetics has been
summarized by the psychologist Eric Turkheimer: “The nature-nurture
debate is over. . . . All human behavioral traits are heritable.” By
this he meant that a substantial fraction of the variation among
individuals within a culture can be linked to variation in their
genes. Whether you measure intelligence or personality, religiosity or
political orientation, television watching or cigarette smoking, the
outcome is the same. Identical twins (who share all their genes) are
more similar than fraternal twins (who share half their genes that
vary among people). Biological siblings (who share half those genes
too) are more similar than adopted siblings (who share no more genes
than do strangers). And identical twins separated at birth and raised
in different adoptive homes (who share their genes but not their
environments) are uncannily similar.
Behavioral geneticists like Turkheimer are quick to add that many
of the differences among people cannot be attributed to their genes.


Identical twins raised apart tend to be almost as similar as identical
twins raised together, although part of the reason is that identical
twins raised alone don't feel the need to distinguish themselves from
their twin by developing something unique about themselves. Horace
Grant, the skinny power forward on Michael Jordan's first three
championship teams, would probably have become a quick forward if he
hadn't grown up playing on youth teams alongside his identical twin
Harvey Grant, who became an NBA All-Star shooting forward, while
Horace was given the role of rebounding forward.

I know two pairs of adult identical twins, the Brimelows and the
Woodhills, and the personal affects vary mildly among the Brimelows
and moderately among the Woodhills.

But not all variation in nature arises from balancing selection.
The other reason that genetic variation can persist is that rust never
sleeps: new mutations creep into the genome faster than natural
selection can weed them out. At any given moment, the population is
laden with a portfolio of recent mutations, each of whose days are
numbered. This Sisyphean struggle between selection and mutation is
common with traits that depend on many genes, because there are so
many things that can go wrong.

Penke, Denissen and Miller argue that a mutation-selection
standoff is the explanation for why we differ in intelligence. Unlike
personality, where it takes all kinds to make a world, with
intelligence, smarter is simply better, so balancing selection is
unlikely.

Is smarter simply better? If it takes, say, bigger brains, the answer
isn't terribly clear. Analogously, Intel assumed that faster
clockspeed computer CPU chips were simply better for about 15 years.
But the struggle to break the 4.0 gigahertz barrier proved
overwhelming and so Intel has given up and gone in different
directions in recent years, when most chips sold seem to be between
2.0 and 3.0 gigahertz, although performance keeps improving.

Keep in mind that Intel has big advantages over natural selection in
getting from one performance peak to another. For example, if Intel
decides that its strategy of single chips with ever faster clockspeeds
is heading toward a deadend, it can simultaneously start working on an
R&D project for double core and quad-core chips with moderate
clockspeeds. At first, the new type of CPUs won't be as good as the
old type, but it doesn't have to sell the beta versions of the changed
design. It can keep making them and throwing them away until the new
style chips are as good as the competition's old style chips.

In contrast, natural selection doesn't provide you much of a
laboratory in which to putter around while you're working the kinks
out of your next model while your factory keeps churning out the
satisfactory current model.

Similarly, bigger brains require more food. They make you more likely
to tip over and hurt yourself. They require your mother to have a
wider pelvis so she won't die in childbirth, which makes her a slower
runner.

But intelligence depends on a large network of brain areas, and it
thrives in a body that is properly nourished and free of diseases and
defects. Many genes are engaged in keeping this system going, and so
there are many genes that, when mutated, can make us a little bit
stupider.

At the same time there aren’t many mutations that can make us a
whole lot smarter. Mutations in general are far more likely to be
harmful than helpful, and the large, helpful ones were low-hanging
fruit that were picked long ago in our evolutionary history and
entrenched in the species. One reason for this can be explained with
an analogy inspired by the mathematician Ronald Fisher. A large twist
of a focusing knob has some chance of bringing a microscope into
better focus when it is far from the best setting. But as the barrel
gets closer to the target, smaller and smaller tweaks are needed to
bring any further improvement.

The Penke/Denissen/Miller theory, which attributes variation in
personality and intelligence to different evolutionary processes, is
consistent with what we have learned so far about the genes for those
two kinds of traits. The search for I.Q. genes calls to mind the
cartoon in which a scientist with a smoldering test tube asks a
colleague, “What’s the opposite of Eureka?” Though we know that genes
for intelligence must exist, each is likely to be small in effect,
found in only a few people, or both. In a recent study of 6,000
children, the gene with the biggest effect accounted for less than one-
quarter of an I.Q. point. The quest for genes that underlie major
disorders of cognition, like autism and schizophrenia, has been almost
as frustrating. Both conditions are highly heritable, yet no one has
identified genes that cause either condition across a wide range of
people. Perhaps this is what we should expect for a high-maintenance
trait like human cognition, which is vulnerable to many mutations.
The hunt for personality genes, though not yet Nobel-worthy, has
had better fortunes. Several associations have been found between
personality traits and genes that govern the breakdown, recycling or
detection of neurotransmitters (the molecules that seep from neuron to
neuron) in the brain systems underlying mood and motivation....


But it seems even less plausible to say that more or less of any major
psychological trait is "simply better." We may have our subjective
preferences, but the major personality traits are likely to be ones on
which normal variation doesn't much change average Darwinian fitness
over the generations.

Even if personal genomics someday delivers a detailed printout of
psychological traits, it will probably not change everything, or even
most things. It will give us deeper insight about the biological
causes of individuality, and it may narrow the guesswork in assessing
individual cases. But the issues about self and society that it brings
into focus have always been with us. We have always known that people
are liable, to varying degrees, to antisocial temptations and weakness
of the will. We have always known that people should be encouraged to
develop the parts of themselves that they can (“a man’s reach should
exceed his grasp”) but that it’s foolish to expect that anyone can
accomplish anything (“a man has got to know his limitations”). And we
know that holding people responsible for their behavior will make it
more likely that they behave responsibly. “My genes made me do it” is
no better an excuse than “We’re depraved on account of we’re
deprived.”

Many of the dystopian fears raised by personal genomics are simply
out of touch with the complex and probabilistic nature of genes.
Forget about the hyperparents who want to implant math genes in their
unborn children, the “Gattaca” corporations that scan people’s DNA to
assign them to castes, the employers or suitors who hack into your
genome to find out what kind of worker or spouse you’d make. Let them
try; they’d be wasting their time.
The real-life examples are almost as futile. When the connection
between the ACTN3 gene and muscle type was discovered, parents and
coaches started swabbing the cheeks of children so they could steer
the ones with the fast-twitch variant into sprinting and football.
Carl Foster, one of the scientists who uncovered the association, had
a better idea: “Just line them up with their classmates for a race and
see which ones are the fastest.” Good advice. The test for a gene can
identify one of the contributors to a trait. A measurement of the
trait itself will identify all of them: the other genes (many or few,
discovered or undiscovered, understood or not understood), the way
they interact, the effects of the environment and the child’s unique
history of developmental quirks.


Well said.

On the other hand, as futile as individual genomics is likely to prove
to be relative to current expectations., the Law of Large Numbers
suggests that racial genomics is likely to prove more fertile."


http://isteve.blogspot.com/2009/01/s...me-tested.html